The biochemical lesions which accompany the impaired myocardial contractile function characteristic of pressure overload induced congestive heart failure are incompletely understood. Further, a great deal remains to be learned about the pharmacology of digoxin and vasodilator agents during pressure overload stress. The broad aim of this study is to study the biochemistry of cardiac muscle myosin and troponin and to further characterize the role of these proteins in the normal heart as well as in the myocardium subjected to chronic pressure overload leading to hypertrophy and congestive heart failure. In addition selected aspects of the pharmacology of ameliorating or preventing the contractile defect of myocardial failure will be explored. Adult cats will be used. Pressure overload will be induced by constricting the pulmonary artery such that hypertrophy and congestive heart failure develop. At the time of final study, the hemodynamic status of each animal and the mechanical function of the heart will be determined. Subsequently the myocardium will be excised and biochemical or pharmacological parameters evaluated. It is submitted that the successful completion of these studies will provide insight into the biochemistry and pharmacology of normal and abnormal cardiac muscle.